Chapter 80 Traumatic Brain Injury
PATHOPHYSIOLOGY
Traumatic brain injury (TBI) is a common injury in children and the most common cause of traumatic death. TBI is often caused by a primary injury, and is followed by a secondary injury. The primary injury is the actual trauma itself, because it occurs at the time of impact on the central nervous system and may cause damage and/or death to the brain cells. A hypoxic insult may also cause a primary injury. The secondary injury is caused by the brain’s response to the trauma and evolves over a period of hours to days after the injury. The secondary injury can result in the loss of cerebral autoregulation, development of cerebral edema, and breakdown of the blood-brain barrier. The secondary injury is exacerbated by systemic hypotension or hypertension, ischemia, hypoxia, or hypercapnia.
There are several types of brain injury:
1. Open head injuries are caused by bullets or other penetrating objects, which include but are not restricted to depressed skull fracture(s) with scalp laceration.
2. Closed head injuries are the more common of the two and usually are caused by a rapid movement of the head, during which the brain is forced back and forth within the skullcap. Such injuries are commonly found in motor vehicle crashes, falls, and recreational sports related activities (i.e., football, bicycling).
Brain injuries are also commonly classified in terms of severity (i.e., mild, moderate, severe).
1. Mild brain injury (Glasgow Coma Scale: 13–15) is commonly referred to as a concussion, which may involve a brief loss of consciousness, loss of memory of events immediately preceding and/or following the injury, alteration in mental status at the time of the injury, and/or neurologic deficits that may or may not be transient. Characteristics most common of mild brain injury include physical, cognitive, and/or behavioral, and are listed below.
2. Moderate brain injury (Glasgow Coma Scale: 8–12) results in a loss of consciousness lasting from minutes to hours, followed by days and/or weeks of confusion. This is usually associated with physical, cognitive, and/or behavioral impairments, which may be transient or permanent.
3. Severe brain injury (Glasgow Coma Scale: <8 for at least 6 hours after injury) always results in prolonged loss of consciousness or coma lasting from days to sometimes months, depending on the severity and location of the injury. Diffuse axonal injury (DAI) is a common finding in severe brain injuries on radiographic investigation. DAI is defined as impaired function and gradual loss of some axons, which are the long extensions of a nerve cell that enable such cells to communicate with each other and integrate global function. Such injuries may leave patients with severe and permanent disabilities involving physical, cognitive, and/or behavioral impairments.
INCIDENCE
1. Males are twice as likes as females to suffer head injuries.
2. Concussions are the most frequent type of TBI.
3. Among children ages 0–14 years, 475,000 TBIs occurred each year between 1995 and 2001 in the United States. Of those, 435,000 children were treated for TBI in the emergency department (ED) each year, 37,000 were hospitalized, and 2685 died.
4. TBI is the leading cause of acquired disability in childhood.
5. Causes of TBI vary with age: very young children ages 0 to 4 years had the highest rate of TBI-related ED visits (1035.0 per 100,000 population).
6. Posttraumatic seizures develop in 7% to 12% of children with cerebral contusions.
7. Exposure to guns and access to a loaded firearm increase the risk of unintentional brain injury and death in a child. The unintentional death rate among children 14 years of age and younger is 9 times higher in the United States than in 25 other industrialized countries combined.
CLINICAL MANIFESTATIONS
2. Headache, dizziness, light-headedness, or loss of balance
3. Bleeding or clear drainage from laceration, nose, or ears
6. Irritability and agitation, sleep problems, fatigue, anxiety, depression, emotional lability
7. Loss of consciousness or cognitive impairment, decreased attention span, concentration or mental speed; short-term memory loss
8. Focal deficit including impaired motor function of limbs such as hemiparesis or hemiplegia
9. Decorticate or decerebrate posturing
10. Battle sign—bruising behind ear
11. Raccoon sign—bruising around eyes
12. Increased sensitivity to lights, sounds, or distractions
COMPLICATIONS
Depending on the type, severity, and location of the head injury, deficits may be multiple and include motor, communicative, cognitive, sensory, behavioral, and emotional problems or delay in reaching developmental milestones not yet achieved. A variety of complications involving the nervous system and other organ systems may be seen. These complications can occur from either the primary or secondary injury to the brain.
Primary Brain Injury
Traumatic brain injury (TBI) is defined as a physiologic disruption of brain function resulting from both external (an object striking the head or the head striking an object) and/or internal trauma (the rapid acceleration/deceleration of the brain within the skullcap).
Primary injuries include the following:
1. Concussion results from shearing and stretching forces in the brain that produce no structural damage. This is the least serious type of injury that requires close monitoring for complications. With a concussion, the child usually has a momentary loss of consciousness. Recovery generally takes place within 24 hours, with a return to the preinjury level of activity and orientation.
2. Cerebral contusion is localized brain injury that consists of bruising, tearing, bleeding, and swelling of the brain, with temporary or permanent structural damage. This may occur directly under the area of impact or on the opposite side of the brain as it hits the skull. A contusion causes a disruption of cerebral tissue to varying degrees with possible surrounding edema. Signs and symptoms reflect the extent of injury and blood loss and may include loss of consciousness, mild motor and sensory deficits, changes in visual awareness, seizures, or coma.
3. Skull fractures may take the form of a linear skull fracture in which the dura mater is not penetrated and usually does not require surgery for repair; a depressed skull fracture, in which bone fragments are indented and can affect underlying brain tissue and produce a hematoma or contusion; or a compound skull fracture, in which a laceration and depressed fracture are present. The skull fragment may lacerate the dura as it is displaced into the brain tissue. A basilar skull fracture is a break in the base of the skull that often results in a dural laceration, which may involve drainage of cerebrospinal fluid through the ear or nose.
4. Hematoma is the accumulation of blood under the skull. An epidural hematoma occurs when there is a blood clot that collects between the skull and the dura mater. This is most common in older children and commonly results from a tear of the middle meningeal artery. Clinically, a loss of consciousness may occur, and thus a hematoma should be excluded by radiographic investigation, if there is a basal or temporal skull fracture. Children with this type of hematoma should be assessed for decreased level of consciousness, development of headache, dilation of the pupil on the affected side, and focal deficit such as hemiparesis or plegia. Surgical evacuation of an epidural hematoma is a common treatment if the child is symptomatic, or if the clot is large enough that there is compression of underlying neural tissue. Recovery from an epidural hematoma is excellent if recognized and treated in an appropriate time frame. Symptoms of a subdural hematoma may be delayed for hours or days since the source of bleeding is venous. A subdural hematoma occurs when blood collects between the dura mater and the brain and is often associated with a contusion. This type of hematoma can become life threatening if it compresses vital centers of the brain or causes cerebral edema. Children with this type of hematoma should be assessed for loss of consciousness, unilateral pupil dilation, focal seizures, and/or hemiparesis. Treatment for symptomatic hematomas, no matter where they are located, is surgical evacuation of the hematoma by a craniotomy procedure. The prognosis for the child with a subdural hematoma is less favorable than that for a child with an epidural hematoma, even after surgical evacuation, owing to the associated damage to the underlying brain tissue.
5. Subarachnoid hemorrhage results from a tear of the subarachnoid arterial vessels resulting from large shearing forces encountered during a severe TBI. It appears as diffuse blood spread thinly over the surface of the brain. This type of hemorrhage is frequently seen in the abused child, as well as resulting from motor vehicle crashes and falls. Children should be assessed for nuchal rigidity, headache, decreasing levels of consciousness, and retinal hemorrhages.
6. Diffuse axonal injury is frequently seen in children with severe head trauma, such as those with shaken baby syndrome and those who have been involved in a motor vehicle crash. This may result in a generalized global decline of the neurologic exam, affecting mental status, motor function, and brain stem function. This type of injury may result in widespread cerebral edema, neuronal dysfunction, and prolonged coma. The prognosis for this type of injury ranges from moderate disability to death.
Secondary Brain Injury
Secondary brain injury results from the severity of the primary brain injury and may be made worse by hypotension, hypertension, deoxygenation, and ischemia. Consequences of secondary injury include the following:
1. Cerebral edema either is caused by the primary injury or is a result of hypoxia, hypercapnia, or cerebral ischemia. Edema usually peaks in 24 to 72 hours after injury, and often results in a deterioration of neurologic status. Cerebral edema may result in increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP); if adequate intervention is not taken, this may result in irreversible brain dysfunction, herniation, and death, if not treated.
2. Meningitis may result from an infection of the cerebrospinal fluid (CSF). Clinically, the child will develop fever, decreased level of consciousness, nuchal rigidity, and irritability; sampling of the CSF will reveal a pleocytosis of the white blood cells.
LABORATORY AND DIAGNOSTIC TESTS
1. Radiographic study of skull—to identify fractures
2. Computed tomography (CT) scan of brain—to identify hematomas, edema, increased ICP, DAI
3. Magnetic resonance imaging (MRI) of brain—to identify hematomas, edema, increased ICP, DAI
4. Test for presence of glucose in drainage from ears or nose—identification of CSF leak
MEDICAL MANAGEMENT
Management goals are to avoid, prevent, and minimize secondary injury to the brain. As with any severe injury, the first step of treatment is management of the airway, breathing, and circulation. Treatment is then based on the neurologic assessment, which includes use of the pediatric Glasgow Coma Scale (GCS). The GCS rates the child’s performance in three major areas: eye opening, motor response, and verbal response. The highest score that can be achieved is 15 (least injured); the lowest is 3 (poorest outcome). Scores of 8 or lower indicate a severe brain injury; scores of 9 to 12 indicate a moderate injury; and scores of 13 to 15 indicate a minor injury.
1. Minor injury (GCS score of 13 through 15) with normal radiologic studies and vital signs. It is recognized that a small percentage of children with normal exams and absence of other findings may still have positive radiographic findings, such as contusion or small epidural or subdural hematoma. It is therefore recommended to perform a head CT scan to exclude this possibility. In the absence of such findings, a child may be discharged to a reliable, knowledgeable parent. Appropriate discharge instructions include the following:
2. Moderate injury (GCS score of 9 through 12): child should be admitted for observation even if radiologic studies are normal. Frequent neurologic checks should be performed and an additional surveillance CT scan obtained if symptoms develop.
3. Severe injury (GCS score of 3 through 8): child should be admitted or transferred to a pediatric intensive care unit. May require surgical evacuation of subdural or epidural hematoma or craniectomy to allow for brain swelling, along with supportive management. ICP monitoring and CSF drainage is generally indicated to monitor and manage cerebral edema. Fluid management, sedation, chemical paralysis, and hyperosmolar therapy are all current modes of head injury management.
In all cases of TBI, the goal of therapy is a return of function. In some cases, function is lost or limited, which results in disability. Factors most predictive of disability(s) in a severe injury include the GCS motor score 3 days after injury, level of oxygenation in the ED, presence of intracranial hematoma, duration of ICP elevation and decreased CPP, and presence and severity of extracranial injuries. Children with a severe injury will require an intensive rehabilitation program designed to promote a return to an optimal level of function. This is best managed in a pediatric inpatient rehabilitation unit, followed by outpatient therapy. In addition to rehabilitation of lost physical function such as impaired motor skills of the upper and lower extremities and language and swallowing abilities, cognitive rehabilitation is also critical to minimize the severity of disability. If a child’s development is in progress before the head injury, cognitive impairment as a consequence of head injury may further limit or impair completion of developmental milestones. For children, a return to school is a major goal. For those with a severe TBI, a special individualized education plan (IEP) will have to be developed to continue with the cognitive rehabilitation. Children may also be provided with school-based physical, occupational, and speech-language therapies; services for the hearing and visually impaired; behavior management; and counseling.
NURSING ASSESSMENT
1. Assess airway, breathing, and circulation.
2. See the Neurologic Assessment section in Appendix A.
3. Assess level of consciousness.
4. Assess for signs of increased ICP such as new onset of irritability, nausea, vomiting, or focal deficits.
5. Assess for skin bruising or swelling, rhinorrhea, or ear drainage.
6. Assess cause of injury and identify potential child abuse.
NURSING INTERVENTIONS
1. Ensure that patent airway, breathing, and circulation are present. Maintain adequate oxygenation using pulse oximeter or other oxygen-saturation monitoring device, and suction at bedside.
2. Monitor for, prevent, and intervene in case of increased ICP.
3. Ensure safe environment, using safety restraints as necessary or chemical sedation.
4. Maximize pain control by identifying agents that will minimize patient’s pain source and limit effect on neurologic assessment.
5. Assess for signs and symptoms of disability.
6. Apply ice to areas of soft tissue swelling, lacerations, or other areas of bruising.
7. Administer skin care under cervical collar, if used.
8. Promote team participation within child’s care to include physical, occupational, and speech therapy assessments and interventions as necessary.
9. Educate child and parents about causes and prevention of TBI.
Discharge Planning and Home Care
Preventive Care
Instruct children and family about importance of prevention. Examples include use of helmets in sports in which injury to head is possible following a fall, prevention of pedestrian–motor vehicle or bicycle–motor vehicle accidents, and avoidance of high-risk behaviors in older children. Offer both oral and written instructions, because families can be overwhelmed at discharge.
Long-Term Care
1. Educate patient and family regarding the need for and administration of medications, particularly antiepileptic (AED) medications.
2. Identify need for outpatient physical and occupational therapy, cognitive retraining, expressive and receptive language retraining, oral motor retraining (speech therapy), behavior management, and counseling.
3. Support child and family with the school reentry process.
Adelson PD, Bratton SL, Carney NA. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Pediatr Crit Care Med. 2003;4(3 Suppl):S72. Lippincott, Williams & Wilkins
American Association of Neurological Surgeons: Traumatic brain injury, What is neurosurgery?. (serial online) www.neurosurgerytoday.org/what/patient_e/head.asp
Brain Injury Association of America [(website):] .Brain injury: The ABC years; Understanding and preventing pediatric brain injury, 2006. www.biausa.org. Accessed June 14
Centers for Disease Control, National Center for Injury Prevention and Control [(website)] .Traumatic brain injury in the United States: Emergency department visits, hospitalizations, and deaths, 2006. www.cdcgove/nicpc/pub-res/TBI_in_US_04/TBI_ED.htm). Accessed June 14
Centers for Disease Control, National Center for Injury Prevention and Control: What is traumatic brain injury?. (website): www.cdc.gove/ncipc/tbi/TBI.htm)
Centers for Disease Control, National Center for Injury Prevention and Control [(website)] .Overview, 2006. www.cdc.gov/ncipc/tbi/Overview.htm. Accessed June 14
